The devastating social, medical, and economic effects of alcoholism have intensified the need to understand the neurochemical mechanisms underlying alcohol self administration and dependence. Studies in animals and in vitro systems have produced increasing evidence that the GABA- benzodiazepine receptor complex (GBRC) mediates some of the pharmacological and behavioral effects of ethanol, especially the genetic variability in ethanol response. Furthermore, recent studies from our laboratory in which we have used PET to directly examine regional brain glucose metabolism in the brains of normal male subjects and recently detoxified male alcoholics (Volkow et al. 1993) support the involvement of the GBRC as a neurochemical substrate in alcoholism. Purpose: Specific aim 1 To investigate the activity of GBRC mediated inhibitory neurotransmission in normal controls and recently detoxified alcoholics; Specific aim 2 To examine the influence of the time period of alcohol withdrawal on GBRC mediated inhibitory neurotransmission; Specific aim 3 To examine the influence of the time period of alcohol withdrawal on regional brain glucose metabolism during baseline.